Investigation of the effects of different biotin forms on miR-21, miR-107 and miR-122 and PI3K/Akt signaling pathway in experimental multiple sclerosis induced rats

The most common neurological disease Multiple Sclerosis (MS), is caused by myelin sheath damage to immune system and central nervous system structures. Biotin supplementation delays the progression of MS and improves the life quality of individuals. Magnesium (Mg) plays a role in the uptake and release of neurotransmitter substances transmitted in nerve cells. Yet, no studies found in the literature on combining Biotin and Mg. In this study, the effects of Biotin and Magnesium-Biotinate (MgB) were investigated, after lysolecithin (LPC) induced demyelination in the experimental MS model. Total 42 Wistar albino rats were divided into 6 groups. i:Control; rats given a single dose of 0.9% saline. ii:LPC; given a single dose of 1% prepared LPC in 0.9% saline. iii:LPC+BI; rats given LPC and 0.9 mg d-biotin. iv:LPC+BII; rats given LPC and 9 mg of d-biotin. v:LPC+MgBI; rats given LPC and 0.9 mg of MgB. vi:LPC+MgBII; rats given LPC and 9 mg of MgB. Biotins were given orally daily for 7 weeks. The expression of miR-21 increased in the LPC group compared to the control and treatment groups, while expression of miR-107 and miR-122 decreased (p<0.0001). While the levels of LPC groups decreased in PI3K, Akt1, Nrf2, HO-1 and Bcl-2 protein levels compared to the control and treatment groups, the protein levels increased in NF-ĸB, Bax and Caspase-3 protein levels (p<0.0001). Eventually, MgB supplementation is anticipated to prevent the progression of MS in rats with LPC-induced MS disease through modulating miR-21, miR-107, and miR-122, NF-ĸB, Nrf2/HO-1, and apoptotic signaling pathways.